The present invention relates to implantable stimulation devices and more particularly to implantable pacemakers that automatically adjust their AV delay and/or PV delay (i.e., interchamber delay) to improve hemodynamics. The invention also relates to methods of adjusting an AV delay and/or a PV delay.
The heart is a four-chamber pump composed of two atria and two ventricles. The atria function principally as entryways to the ventricles, but they also pump weakly to help move the blood on through the atria into the ventricles. The ventricles supply the main force that propels the blood through the lungs and through the peripheral circulatory system.
At an appropriate time, which is determined by a sino-atrial or xe2x80x9cSAxe2x80x9d node, an a periodic spontaneous electrical depolarization is provided which causes the muscle tissue surrounding the atrium to depolarize. Depolarization of the atrial muscle tissue can be monitored by detecting an electrical signal reflective of atrial depolarization known as a P-wave.
Subsequent to the occurrence of the P-wave, the atrial muscle contracts and forces blood from the atrium into the ventricle. The SA node stimulus that caused the atrium to depolarize also travels to the ventricle and the atrioventricular or xe2x80x9cAVxe2x80x9d node through the AV bundle.
The AV node is neuromuscular heart tissue in the lower middle part of the right atrium. It receives the impulse to contract from the SA node, via the AV bundle, and transmits the impulse through a Purkinje bundle of pathways to the ventricles. The Purkinje bundle is composed of neuromuscular heart fibers that pass from the AV node forward to the septum between the ventricles, where it divides into right and left bundle branches, one for each ventricle. The fibers thus transmit the SA node stimulus from the atria to the ventricles.
As the SA node stimulus travels through the heart, it is typically delayed by the AV node by an amount that corresponds to the time it takes the blood to flow from the atrium to the ventricle. After the delay (natural conduction time of the heart), the conducted depolarization arrives at the ventricular muscle tissue, which causes the ventricular muscle tissue to depolarize.
Depolarization of the ventricular muscle tissue is manifest in the occurrence of an electrical signal known as the QRS-wave complex, which shows the depolarization of the muscle tissue along the heart""s septum. For simplicity, one may easily use the largest amplitude signal from the QRS wave complex to monitor the occurrence of the QRS signal. This major signal, which relates to the major septum depolarization, is the xe2x80x9cRxe2x80x9d wave.
Immediately following this depolarization, the ventricular muscle tissue contracts and forces the blood through arteries to various body locations. The ventricular muscle tissue then re-polarizes and begins to relax. Immediately prior to ventricular re-polarization and relaxation an electrical signal may be sensed in the ventricular muscle tissue, known as the xe2x80x9cTxe2x80x9d wave.
In this manner, the heart pumps blood by having the atria contract at a rate determined by the SA node, and after the natural conduction time, by having the ventricles contract. After a period of time, when the atrium has refilled with blood returning from throughout the body, the process repeats.
The process wherein the atria and ventricles sequentially depolarize and contract in order to pump blood and get ready to depolarize again, is called the cardiac cycle. A given cardiac cycle thus includes one P-wave (or equivalent atrial activity evidencing depolarization of the atria), one QRS-wave (or equivalent ventricular activity evidencing depolarization of the ventricles) and one T-wave (or equivalent ventricular activity evidencing re-polarization of the ventricles).
An implantable stimulation device is an implantable medical device that monitors the activity of the heart for the occurrence of P-waves and/or QRS-waves, and steps in with electronically generated stimuli, when needed, to force the depolarization of the atria and/or ventricles.
A generated stimulus that is delivered to the atrium from an implantable stimulation device is referred to as an A-pulse. A stimulus that is delivered to the ventricle is referred to as a V-pulse. Most implantable simulation devices are configured to provide an A-pulse and/or V-pulse only if a prescribed period of time has elapsed without the occurrence of a P-wave and/or an R-wave, i.e., without the occurrence of natural heartbeats.
The period of time between depolarization of the atrium and depolarization of the ventricle is referred to as the PQ or PR interval. For most dual-chamber implantable stimulation device modes of operation, the device will only generate an A-pulse at the conclusion of an atrial escape interval, and only if a P-wave does not occur during the interval.
The length of time (which is programmable in most implantable stimulation devices) between an atrial paced event, and the delivery of a ventricular output pulse, is referred to as the AV delay or AV interval. An AV delay may be terminated, i.e., a ventricular pulse will not be delivered to the heart""s ventricle by the implantable stimulation device, if an intrinsic ventricular event, an R wave, is sensed before the AV delay times out.
The PV delay or PV interval is the time period from the onset of the intrinsic P wave (atrial depolarizaton) to the ventricular pacing stimulus. The AV delay and the PV delay are measured in milliseconds. An implantable stimulation device, for most modes of operation generates a V-pulse only if the PV delay elapses after atrial activity without the occurrence of an R-wave. The heart is thus afforded as much time as practical to beat on its own before the electronically-generated stimuli of the pacemaker are delivered to the heart, causing the ventricle to contract.
In the prior art, when an Implantable stimulation device is implanted in a patient, or thereafter, the value of the AV delay and/or PV delay can be set to a value that is selected to optimally assist the patient""s heart as it performs its critical function of a pump. For many patients, such an AV/PV delay value is a value that is somewhat longer than the natural conduction time of the heart. This affords the patient""s heart as long a time period as possible before delivering a stimulation pulse.
However, for other patients, it may be desirable to set the AV delay for the implantable stimulation device at a value that is less than the natural conduction time of the heart, thereby assuring that a V-pulse is preemptively generated with most every cardiac cycle.
While the AV/PV delay of a pacemaker can be programmably set to a desired value, the natural conduction time of the patient may vary, either with time, or with the medical or physiological condition of the patient. For example, the natural conduction time may vary as a function of whether the patient is undergoing physiological stress (e.g., exercise), or whether the patient is under the influence of medication.
In most instances, it would be desirable to have the AV/PV delay of an implantable stimulation device closely mimic the natural conduction time of the heart, because such natural conduction time represents the natural timing between depolarization of the atria and depolarization of the ventricles.
Moreover, many patients who suffer from congestive heart failure have hearts that still have suitable conduction, but that do not have sufficient hemodynamic results. Implantable devices have attempted to improve the hemodynamic output of such patients by providing biventricular stimulation. Others methods of improving the hemodynamics in patients that suffer from congestive heart failure are needed.
What is described herein is a device and method that dynamically adjust the AV delay and/or PV delay to improve hemodynamics.
The AV and/or PV delay of an implantable stimulation device is adjusted to cause fusion of the externally provided ventricular pacing stimuli with the patient""s own natural conducted cardiac rhythm.
In one embodiment, biventricular pacing is eliminated, and a single left ventricular lead to provide all ventricular pacing. In this embodiment, a system and apparatus are provided to adjust the atrioventricular delay (i.e., the AV and/or PV delays) to achieve fusion between the left ventricular paced event and the naturally occurring R-wave.
In one embodiment, the AV/PV delay is adjusted by using morphology of the ventricular evoked response as a metric of fusion. Thus, the optimal AV and PV delays are automatically adjusted based on a servomechanism that causes fusion of the evoked response with the naturally occurring heartbeat.
The construction and method of operation of the device disclosed herein will be best understood from the following description of specific embodiments when read in connection with the accompanying drawings.